EN14: What are the limits to evolution?

In Darwin’s Black Box: The Biochemical Challenge to Evolution, biochemist Michael Behe explained how so many of life’s structures and processes are irreducibly complex. He made a slam dunk case for Intelligent Design (ID), while documenting the abysmal lack of any peer-reviewed scientific research that has ever addressed how cilia, flagella, the blood clotting system, or the immune system, to name just some examples, could have “evolved” by the Darwinian process of mutations and natural selection. (I reviewed this book in a previous blog.)

In short, Behe made it clear that the evidence for ID in life is overwhelming, while at the same time showing that there exists no theory of evolution at all regarding life at the cellular level. It’s not that evolution is “wrong.” It’s worse than that. It’s that there simply is no theory of evolution. Just stories . . . word games . . . as Behe documents in representative cases.

Eleven years later, in 2007, Behe published The Edge of Evolution: The Search for the Limits of Darwinism. He takes advantage of the compelling progress in the previous decade regarding the understanding of life at the cellular and nano-structural level to extend his arguments. I want to discuss what I see as two major themes in the book. The second theme centers on what Behe half-jokingly terms, “irreducibility squared.” The cilium has turned out to be far more complex than Behe and other biochemists thought in the 1990s. The cilium serves as a nanotechnology outboard motor, integrating 200 different kinds of proteins in a wonderfully efficient dynamic structure. What is more amazing than the cilium itself is the brilliantly controlled manufacturing / construction process a cell employs to build a cilium and maintain it. The discovery of that process has shocked biochemists due to its sophistication.

But let’s start with what I think is the primary theme of the book. The author sets out to estimate the practical limits of the classical Darwinian process of mutation and natural selection. Everyone engaged in the Creation (or ID) vs. Evolution debate is well aware of the “best examples” cited ad nauseum by evolutionists: for example, bacterial resistance to antibiotics.

Can microbes “evolve” to survive attacks by drugs that target the invader’s ability to metabolize or reproduce or perform some other vital function? Sure. But how? Is this “evolution” a constructive process that, in principle, is on the road to stronger microbes, leading then to multicellular creatures and invertebrates, fish, reptiles, mammals, and man? Or is the “evolution” in question merely a destructive process, leaving the organism weaker, but fortuitously resistant to the very particular threat from that particular drug? The answer is . . . destructive, weaker . . . yet a con game is employed by evolutionists who insist that “destructive evolution” is the same process that produced all of Earth’s biosystems.

The most compelling case to study here is the everlasting war between malaria and humans. As Behe writes, “Because it has been studied so extensively, and because of the astronomical number of organisms involved, the evolutionary struggle between humans and our ancient nemesis malaria is the best, most reliable basis we have for forming judgments about the power of random mutation and natural selection. Few other sources of information even come close. And as we’ll see, the few that do tell similar tales.”

So let’s talk about malaria. To get into the other “similar tales” that Behe cites, please read his book! In some parts of the world malaria kills half of all children before they reach five years of age. Overall, it kills about a million people every year. In the mid-twentieth century, “miracle drugs” were developed that produced hope that a permanent cure was at hand. But mutant strains of malaria survived these drugs and rendered them impotent.

The single-celled malarial parasite is carried by mosquitoes and circulates in our bloodstream until it reaches the liver, where it multiplies exponentially. Re-entering the bloodstream, a next generation malarial cell grabs a red blood cell, enters it, and feeds on hemoglobin (which is the protein nanostructure that carries oxygen for us). One malarial cell becomes twenty, which break out and attack other red blood cells. In a few days a trillion new parasites can form and destroy most of a victim’s blood.

Some humans over the ages have suffered a mutation in the “beta chain” of hemoglobin, a single amino acid substitution at position 6 out of the 146 amino acids in the chain. (The protein hemoglobin is a precisely folded structure consisting of two alpha chains and two beta chains woven together.) The disease is called “sickle cell anemia,” and afflicts millions of people of African descent.

The mutation distorts the hemoglobin structure, causing one protein to stick to another and another, producing a messy blob inside the red blood cell. This distorts the shape of the cell and inhibits its passage through capillaries. Tissues can die and pain can be severe. The spleen gets involved, though, and destroys cells it recognizes as abnormal.

The genetics of the mutation means life or death. People who carry the sickle cell gene from one parent, but not both, experience non-fatal effects. Only half of their blood’s hemoglobin is in the sickle form and they can enjoy good health. But when two carriers mate, each child has a one in four chance of getting the full blown disease.

What happens when malaria attacks the blood of a sickle carrier? When the parasite feeds inside a red blood cell, its enzymes provoke the hemoglobins to glob up, distorting the cell quickly, which is then destroyed by the spleen. Wonderful! The parasite dies, too. Being a carrier – but without the full blown disease – is advantageous in a malaria-infested region. Those that have the full disease, of course, are already in deep trouble. Their damaged hemoglobin coagulates spontaneously, without any push from a parasite.

Thus mutation and natural selection, while damaging hemoglobin and fostering a deadly disease, has produced populations in Africa that are resistant to malaria, albeit at a huge cost. Evolutionists often opine that this is an example of an “arms race,” akin to the Cold War competition between the U.S. and the Soviet Union. One side develops better missiles and the other responds with missile defense systems, provoking development of technology to fool the missile defenses, and so on. But an arms race entails the design of more advanced systems, an ever-upward technological path. The competition between malaria and humans has no such characteristic. It’s much more like trench warfare, featuring attrition and destruction.

Behe offers an analogy of a city under attack. The defenders destroy the bridges to keep the invaders on the other side of the river. The city is clearly not more functional without its bridges, but there is an advantage when an invader is at the door. Similarly, a home invader may be kept at bay by welding the door locks closed. All the evolutionary stories that can be supported with evidence at the biochemical level are of this kind.

The author argues on mathematical grounds that the sickle cell mutation may have arisen only once in human history or, at best, just a few times. He notes that “even in the professional literature sickle cell disease is still called, along with other mutations related to malaria, ‘one of the best examples of natural selection acting on the human genome.’”

One of the best examples? Really? Yet this example is about de-volution, not at all the kind of process that could be relevant to the construction of new, complex, and intricate structures and processes, like cilia and blood clotting. Note additionally that the sickle mutation is not an improvement of the immune system – the biochemical system that functions to fight off disease. The mutation effects a corruption of the circulatory system. As Behe states, “Using hemoglobin to fight off malaria is an act of utter desperation, like using a TV set to plug a hole in the Hoover Dam. Even leaving aside the question of where the dam and TV set came from – which is no small question – it must be conceded that this Darwinian process is a tradeoff of least-bad alternatives. The army in its trenches is suffering loss upon loss. No matter which way it turns, in this war fought by random mutation and natural selection, it is losing function, not gaining.”

You may choose to use the same word — evolution — to describe sickle resistance to malaria, on the one hand, and goo-to-you-via-the-zoo, on the other hand, but you would not be honest in doing so, would you?

Behe points out that it is a lot tougher to build complex machines than to wreck them. It’s easier to throw a wrench into a high performance jet engine than to build the engine in the first place. And so it is in the complex biochemistry associated with the invasion and attack of parasites. The book goes on to describe a number of other mutations in the human genome that help to thwart the lethality of malaria. In every case, though, the normal efficient functioning of human proteins is corrupted, leaving us weaker than before. The conclusion is obvious: “Sickle hemoglobin itself is not an advancement of the immune system; it’s a regression of the red blood cell.”

What about the other side in the conflict? In the 1930s a synthetic drug, chloroquine, was developed by a German pharmaceutical firm. For decades it was a wonderful prescription for fighting malaria. But more and more patients over time failed to respond to the drug. By the 1980s chloroquine was almost completely ineffective against malaria. What happened?

When the parasite feeds, it cannot digest the heme part of hemoglobin, which becomes a toxic waste product that is chemically neutralized within the attacker’s “stomach.” Chloroquine interferes with this neutralization process, heme accumulates, and the bug dies. Justice is served! Now, the malaria genome encodes for 5300 different proteins. One of them, PfCRT, is a protein pump. Protein pumps push selected molecules through particular membranes in cells. PfCRT has 424 amino acids. Long, painstaking research has identified that mutant strains of malaria that are resistant to chloroquine have two point mutations in this particular protein pump, one at position number 76 and another at 220. It appears that this double mutation has arisen twice, once in South America and a second time in Asia.

The mutated protein pump apparently allows the chloroquine to leak out so that it can’t effectively damage the bug’s waste removal system. The rare mutants survive drug programs and reproduce prolifically. You can kill a trillion “normal” parasites, but if one mutant survives, that single one can re-generate a trillion offspring quickly. Thus mutation and natural selection explain the global victory of malaria over chloroquine. But is malaria more complex now? Is it building more sophisticated protein machines or control systems? Evidence indicates that in the absence of chloroquine, the original parasite, with its healthy pump, readily out-competes the mutant strain. Once again, we have de-volution, not a process wherein new complexity is built.

Note that chloroquine resistance involves the simultaneous mutation of two amino acids, as opposed to sickle, which requires merely one. This explains why the drug was effective for decades. The odds against a specific double mutation are exponentially greater than for one. Behe cites the case of atovaquone, an anti-malarial drug that can be defeated by a single point mutation in a single gene. About one in a trillion parasites naturally own this mutation. But the double mutation that defeats chloroquine naturally occurs only once in 1020 bugs.

That sounds like long odds, but there are an enormous number of parasites in a victim’s body – about a trillion – and about a billion people get infected in the world every year. So several mutant parasites occur spontaneously every year. Behe calls the required double mutation a CCC – a “chloroquine complexity cluster.”

Let’s now apply these real-life Darwinian examples to the evolution of life on Earth. If you’re an evolutionist, you believe that humans and chimps split from a common ancestral line perhaps 10 million years ago. The total number of humans in world history would be perhaps a trillion. (For a creationist, the number since Adam would be about 10 billion.) The number of humans – 1 trillion – is a factor of 100 million smaller than the odds against a double mutation like a CCC (1 in 1020). Thus we would expect to have to wait 100 million times 10 million years to achieve a mutation in the human genome comparable to a CCC in malaria. That’s way, way, way past the assumed evolutionary age of the universe. Therefore, even in the alleged last 10 million years, there cannot have been one mutation as complex as a CCC in the line leading to humans. (Large creatures, like mammals, have smaller populations and longer generation times than microbes. Therefore, they simply cannot evolve as fast.)

Behe then extrapolates to the alleged evolution of the 5,000 species of mammals, including the spectacular diversity represented by bats, whales, kangaroos, and elephants . . . “Yet that entire process would – if it occurred through Darwinian mechanisms – be expected to occur without benefit of a single mutation of the complexity of a CCC.”

The author goes on to deal with expected objections to his analysis. I heartily encourage you to read his analysis and decide for yourself whether the arguments are reasonable. Then he extrapolates one more time. What if an environmental challenge arose during the course of life’s history on Earth that necessitated a cluster of mutations twice as complex as a CCC – a double CCC? In that case, the odds against it would be the square of 1020, namely one in 1040. That’s how many cells you would need to get an even chance for a double CCC to occur once. A reasonable estimate is that during the entire course of “evolutionary history,” 1040 exceeds the number of cells that have ever lived on Earth.

In short, that is the “edge of evolution.” If any protein structure or genetic control system requires more than a double CCC, it’s just too bad. It won’t evolve! And, as Behe says, “life is bursting with such features.” Thus “evolution” can have nothing to do with the origin and development of life, with all of its brilliantly complex systems.

This moves us to the second major theme of the book, compellingly illustrated with discoveries uncovered on the cilium. The cilium is an undulating whiplike structure that extends from a cell’s body. It can be smaller or very much larger than the rest of the cell. Examples include . . .

Cilia are found in the lining of the windpipe to sweep mucus and dust out of the lungs. The beating of cilia in the Fallopian tubes moves a fertilized egg from the ovary to the uterus. Without such cilia, human beings cannot reproduce! The tail of a sperm cell is a modified cilium. Sperm that don’t swim well don’t win the prize. Cilia are also vital in embryology, including the embryological development of vertebrate retinas.

Where “irreducible complexity squared” comes into play is that the construction of a major cellular structure like a cilium requires the same – or more – planning than does the building of a skyscraper. Behe concludes “more planning” because the entire process must be carried out by unseeing molecular robots rather than the conscious construction workers, foremen, engineers, and architects who build structures in our cities.

In the 1990s researchers discovered a process now called “intraflagellar transport” (IFT). (It applies both to cilia and flagella, but ‘flagella’ got picked for the name.) IFT is a system of machines and processes that build and maintain the cilium. If a cilium is cut off, it will be rebuilt in about an hour. Little IFT rafts, like boxcars, move up and down the growing structure. Just like building a skyscraper, materials are brought to a staging site near the base, just the right materials at just the right time.

Behe asks what it would be like if all the materials of a building were brought all at once or at random to a construction site . . . all the plumbing, wiring, paint, plaster, desks, girders, etc. What a mess! It takes experienced construction workers to keep the job progressing efficiently. Similarly, but all automatically, the right materials for the cilium must arrive in the proper order, loaded onto an IFT raft, offloaded at the right level, and installed perfectly. A typical cilium contains about 200 different kinds of proteins, which must be hooked together to form this controllable undulating motor which the cell needs to do its job.

Recalling the irreducible complexity of the simple mousetrap described in Behe’s first book, he points out that a much tougher problem would be to explain the origin . . . without human intervention . . . of an automated mousetrap factory. All the materials must be brought to the factory which then fashions the components with precision, and then assembles, fashions, and delivers finished mousetraps. Frankly, human technology is not advanced enough to construct such a factory, that maintains itself reliably and indefinitely.

How much more challenging the problem of automated cilium construction and maintenance. Maintenance? The IFT system operates throughout the cell’s life, refreshing the materials within the cilium. Skyscrapers don’t do that . . . not autonomously, at least!

The cilium is just a representative of the many complex structures in any cell. Can such structures be formed by random mutations? Malaria has never been able to deal with the single amino acid change of sickle hemoglobin. That’s just a single point mutation! The construction of the hundreds of protein machines in cilia and the hundreds (at least) of genes associated with IFT go many orders of magnitudes beyond a single mutation . . . or a CCC . . . or a double CCC.

If a double CCC cannot happen in the history of the universe, then how long must it take for the millions of constructive and simultaneous mutation / natural selection events necessary for the complex nanomachines of the cell?

Evolution is sunk without a trace. Worse, there is no theory of evolution. The only examples of Darwinian evolution consist of trivial destructive examples, like sickle resistance to malaria, and malaria resistance to chloroquine. There is nothing on the “positive side of the ledger.” Yet cellular systems like IFT, cilia, flagella, blood clotting, and the immune system are not built from one or two amino acid changes. These are systems that reflect systems of genes and proteins consisting of tens of thousands of nucleotides and amino acids, as finely tuned (or more so) as any sophisticated machine . . . or automated factory. Biological subsystems require dozens of different protein machines operating in coordination. Evolution – mutation / natural selection – has nothing to do with all this.

Machines . . . processes . . . functions . . . coordination . . . technological sophistication . . . all speak to a Designer, a Creator. Only God will do. It’s just not hard to figure out, unless you are predisposed to avoid the conclusion at all cost.

Behe goes on to describe how every major cellular process is carried out by assemblies of 6 or more protein molecules. Each of these protein assemblies, in turn, interacts with several other large complexes of proteins. The entire cell is akin to a factory containing an elaborate network of interactive assembly lines. How proteins interact with each other is determined by the shape of their convoluted surfaces. The part of a protein molecule’s surface that interacts with another’s is termed a “binding site.”

To change the shape of a binding site in a coherent way so that it might fit effectively with a different protein, and enable a new function, perhaps, requires at least five or six precise amino acid substitutions. Behe goes through the numbers again, and points out that the probability for getting two new binding sites (for a new, novel pair of proteins) is equivalent at best to a “double CCC,” less than one in 1040 . . . a number greater than all the cells that could have ever existed on Earth.

Therefore, such evolutionary novelties are statistically – scientifically – impossible. Furthermore, “the great majority of proteins in the cell work in complexes of six or more.” The edge of evolution . . . the limit of evolutionary ‘creation’ . . . is woefully restricted. The word “evolution” should not be associated with any functional biological structure or function or life form.

Behe is not a creationist. He believes in billions of years, common descent, and intervention at critical times by a designer. Since he is a Roman Catholic, that would be the RC god who exalts church tradition above the book of Genesis and anything else in the Bible that’s not convenient.
It’s a shame that he doesn’t apply his substantial reasoning ability to the rest of the creation / evolution conflict.

Behe has an interesting, speculative chapter on multiverse ideas that are promoted to overcome the mathematical futility of Darwinian evolution. He does a great job describing the anti-scientific fallacies of such speculations, but I’ll leave the details to you . . . read the book if you like.

If you get ahold of Behe’s two major themes – (1) the drastically severe limits on mutation / natural selection, and (2) the awesome and irreducible complexity of all of life’s structures and processes – then you will understand evolution better than any evolutionist, even if he has a Ph.D. Yes, really. The committed evolutionist, no matter how well he claims to understand biochemical processes or genetics, draws insane conclusions about the capacity of mutations to produce Earth’s ecosystem. If he gets the conclusion wrong . . . if he gets wrong the most vital aspect of all of God’s creation, then it doesn’t matter whether he is proficient at either word games or bogus math models.

– drdave@truthreallymatters.com

Comments are closed.